Developmental rate and viability of rainbow trout with a null allele at a lactate dehydrogenase locus

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Abstract
We show that a previously described isozyme polymorphism in rainbow trout(Salmo gairdneri) is the result of an enzymatically inactive (i.e., null) allele(n). Ldh3 null homozygotes(n/n) and heterozygotes(100/n) have reductions of about 20 and 12% in total lactate dehydrogenase (LDH) activity at hatching, respectively. As juveniles,(100/n) fish have reductions in LDH activity of 15, 37, and 21% in brain, heart, and white muscle, respectively. Embryos with differntLdh3 phenotypes from 11 families do not differ significantly in either survival or hatching time. However, a second measure of developmental rate, the amount of malate dehydrogenase (MDH) and phosphoglucomutase (PGM) activity in 33-day-old embryos, suggests that(100/n) embryos develop more slowly than(100/100) embryos. In three of four families examined,(100/n) embryos have significantly lower amounts of total MDH activity (8–10%). In one of these,(100/n) embryos also have significantly lower total PGM activity (15%). These data suggest that the reduction in total LDH activity is associated with small but detectable delays in developmental rate but nondetectable differences in survival to hatching.